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					                     The University of Texas Medical Branch
                      The School of Allied Health Sciences
                       The Physical Therapy Department

               PHYT 6202 - Basic Spinal Tissue Pathophysiology

             NTK = Nice to know; not commonly dealt with by PTs
         ETK = essential to know; pathology commonly dealt with by PT.

I. The intervertebral segment
       A. Constituents
              1. Anterior Elements
                     a. Vertebral Bodies
                     b. Intervertebral disk
                     c. Ligaments
                            (1). Anterior longitudinal ligament
                            (2). Posterior longitudinal ligament
                            (3). Interspinous Ligamant
                            (4). Supraspinous Ligament
                            (5). Intertransverse Ligament
                     e. Anterior muscles (Many authors do not include the
                     muscles within the Intervertebral segment)
                            (1). Intersegmental - “deep”, local, (longus colle;
                            Transversus abdominus)
                            (2). Extrasegmental – “global” (Rectus abdominus,
                            sternomastoid)
                     f. Arteries, veins and nerves to these structures.
              2. Posterior Elements
                     a. Bony neural arch
                            (1). Laminae
                            (2). Transverse and spinous processes
                     b. Facets and facet joints and tissues
                     c. Spinal cord and meninges (especially the dura)
                     d. Spinal nerve roots
                     e. Intersegmental muscles – “deep”, local, (multifiidi,
                     rotatores)
                     f. Extra-segmental muscles (iliocostalis, semispinalis, etc)
                     g. Ligaments
                            (1). Ligamentum flavum
                            (2). Interspinous ligament
                            (3). Supraspinous ligament
                     g. Arteries, veins and nerves to these structures
              3. Lateral elements
                     a. Ribs
                     b. Joints of von Luschka
                     c. Intertranverse ligaments
PHYT 6202 - Basic Spinal Tissue Pathophysiology                                     2


                     d. Side flexing muscles – (scalene, quadratus lumborum)

II. Overview of tissue pathology-
       A. Pathological mechanisms of injury: Trauma, Posture (chronic sprain,
       strain and fatigue), Degeneration, Systemic, Combinations
       B. Trauma
              1. Injures mostly the collagenous tissues in spine structures. The
              inflammation and repair processes of collagen in tissue are usually
              what guides treatment and management. The time lines of
              recovery and chances of restoration are different for different types
              of collagenous tissues depending on their constituency and
              function.
              2. Traumatic mechanisms
                      a. Directions of force –
                              (1). Hyperflexion (anterior hypercompression c
                              posterior distraction),
                              (2). Hyperextension – posterior hypercompression c
                              anterior distraction
                              (3). Hyper side flexion to the R – R
                              hypercompression c L distraction and v.v.
                              (4). Hyper rotation to the L – hypercompression of R
                              facet with distraction of R anterior disk and v. v.
                              (5). Combinations (hyperflexion c rotation
                              hyperextension c rotation);
                      (6). Extrincic mechanisms –
                              (1). Surgery
                              (2). Contusion
                              (3). Deep tissue wounding (gunshot wound,
                              penetrating objects).
              3. A good mental exercise for students is to imagine what
              structures might be injured by each mechanism.
              4. In traumatic mechanisms several different tissues are injured
              simultaneously. Return to function is limitated is the "weakest link",
              i.e., the tissue that is injured most easily or severely by the trauma;
              the tissue that heals the slowest or the tissue that less completely.
              These are often cartilage and nerve.

III. Trauma to anterior elements
        A.. Vertebral body compression fracture http://www.medmedia.com/o11/183.htm
        (NTK) - most common is anterior wedge fracture; heal readily in healthy
        host; occur readily in unhealthy host (osteoporosis); Newest treatment is
        vertebroplasty; serious complication is expansion into spinal canal or local
        kyphosis causing spinal stenosis.
        B. Distraction fracture - http://www.medmedia.com/o11/198.htm (NTK) Chance
        fracture; flexion distraction –
PHYT 6202 - Basic Spinal Tissue Pathophysiology                                   3


      C. End plate fracture (see interspongy disk herniation below) (ETK)

      D. Anterior longitudinal ligament sprain or tear
            1. Most often occurs in hyperextension phase of cervical whiplash
            but can occur with hyperextension (hyperlordosis) of the lumbar
            spine.
            2. Early pathology - rupture of collagen fibers and bonds; bleeding
            and inflammation; healing collagen cycle.
            3. Late pathology -
                    a. Collagen may heal with excessive length (most likely)
                    allowing excessive lordosis or with diminished length
                    producing postural dysfunction.
                    b. Excessive length may allow anterior shearing instability
                    leading to facet joint degeneration.
      E. Anterior muscle strain and tear (ETK)
            1. Mechanisms of injury: Hyperextension, hyperextension with
            rotation, sometimes contusion.
            2. Early pathology=
                    a. Strain = more of a collagenous injury; bleeding and
                    inflammation/repair of collagen.
                    b. Contusion = can have contractile element injury as well
                    as collagen; more bleeding and collagen repair; collagen
                    repairs some of contractile element. in contusion, (c).
                    Spasm, antalgic posture and movement
            3. Late pathology = abnormal remodeling; diminished or excessive
            length. May establish postural dysfunction

      F. Disk tear (ETK)
             1. Sudden intense force on a small area of the intervetebral disk
             causes a tear; to get a large force on a small area of the healthy
             disk requires a combination of movement; hyperflexion with
             rotation; can be hyperextension with rotation. In the hyperextension
             with rotation mechanism the facet joint can be injured as well as
             the disk. The facet joint may subsequently become hypomobile
             straining the disk more with function .
                     a. Lumbar - usually postero-lateral from twisting while bent
                     forward; usually lifting, shoveling, etc.
                     b. Cervical - tear of anterior disk with extension phase of
                     acceleration injury.
             2. Immediate pathology
                     a. Release of pain producing substances - Disk is
                     innervated and some pain comes from disk
                     b. When collagen in cartilage is fractured there is a
                     inflammatory response. By products of collagen breakdown
                     can be very irritating to the surrounding structures including
                     nerve roots and dura.
PHYT 6202 - Basic Spinal Tissue Pathophysiology                                       4


                    c. Annulus is made of collagen and elastin; collagen
                    attempts to heal; probably never reconstitutes itself,
                    especially elastin; may heal with fibrous scar but is very
                    slow.
                    d. Because nucleus pulposis is contained by the annulus
                    under pressure, tear might cause torn annulus to
                    immediately protrude; Annulus might rupture immediately
                    and allow NP to prolapse or extrude.
             2. Long term pathology - Disk tear is often not important for what
             immediately results from the disk injury but what might occur over
             time after disk tear. Often leads to other problems:
                    a. Weakens annulus so annular bulge or HNP is more
                    likely over time.
                    b. Loss of one control of rotation at the segment. Annulus
                    helps control rotation (with facets, oblique abdominals, and
                    multifidi mm.) so facets might be injured at same time as
                    disk tear or segmental rotational instability might exist after
                    tear subjecting facets to excess wear.
                    c. Disk space may narrow allowing shearing instability.

      G. "Intraspongy" herniation - (ETK) Nucleus pulposis herniates superiorly
      or inferiorly through weakness in the inferior or superior cartilage end
      plate. Most frequent in the lower thoracic area and upper L/S. Causes
      few acute symptoms. Creates the phenomenon known as "Schmorl's
      nodes".
              1. Results for fall from height into spinal flexion or lifting heavy
              object in hyperflexed position.
              2. Early pathology = healing of bone; fibrosis of invading nucleus.
              3. Late pathology=Because disc narrows and segment becomes
              stiffer segments above and below may develop excessive motion if
              patients movements require full ROM.

      H. To injure the structures named above takes significant force when they
      are healthy. If the same tissues are degenerated, less force can cause
      significant injury.

      I. Circulatory and neural elements - The major neural elements are
      posterior; some anterior ones that can be pathological are:
             1. Vertebral artery (NTK) – also considered a lateral element
             2. Artery of adamkewicz (NTK)
             3. Abdominal aorta (NTK)
IV. Trauma to Posterior Elements
      A. Bone -
             1. fracture of neural arch; see Wheeless textbook of orthopedics
             (NTK) http://www.medmedia.com/o11/145.htm
PHYT 6202 - Basic Spinal Tissue Pathophysiology                                      5


             2. Avulsion fracture of the spinous processes - "Clay shoveler's
             fracture - (NTK) http://www.medmedia.com/o11/143.htm
             3. Isthmic Spondylolysis and Spondylolithesis
                    a. Latest theoretical cause is repetitive stress; patient may
                    have inherited tendency.
                    b. Fracture of pars interarticularis with repetitive
                    hyperextension or hyperextension with rotation.
                    c. Spondylolysis – stress fracture unilaterally or bilaterally
                    without separation.
                    d. Spondylolythesis – separation at fracture site with
                    anterior vertebral slipping of L5 on S1. Slipping graded on
                    how much of L5 overlaps S1.

      B. Ligament sprain (ETK)
            1. Distraction - posterior longitudinal, interspinous, supraspinous
            most often by hyperflexion or combination flexion/rotation. Often in
            cervical spine with hyper-flexion phase of whiplash. Less often in
            thoracic and lumbar spine.
            2. Immediate pathology= inflammation and repair of collagenous
            tissue
            3. Chronic pathology = ligament may remodel with diminished or
            excessive length predisposing segment to acceleration of
            degeneration.
            4. Compression or impingment - Interspinous and supraspinous
            can be pinched by "kissing spinous processes" phenomenon

      C. Facet joint fractures; dislocation - unilateral or bilateral jumped facet
      (NTK) http://www.medmedia.com/o11/110.htm

      D. Facet joint sprain (ETK)
            1. Patient history usually separates this disorder from other non-
            fracture/dislocation causes of facet joint pain. With FJ sprain there
            is a history of trauma. Pain pattern during movement tests agrees
            with direction of capsular stretching force.
            2. Hyper-flexion sprain (ETK)
                    a. Hyper-flexion stretches the posterior joint capsule;
                    Therefore flexion and/or rotation are most painful; extension
                    is better movement. Often postures in increased lordosis or
                    extension and rotation toward painful side.
                    b. Rotation combined with flexion may sprain facet joint
                    unilaterally.
                    c. Short term pathology - collagenous tissue over strain with
                    usual sequelae; may accompany other hyper-flexion or
                    rotation pathology.
                    d. Long term pathology = facet joint hypo-mobility or
                    hypermobility.
PHYT 6202 - Basic Spinal Tissue Pathophysiology                                    6


                   e. Hyper-flexion may have a different pathology when the
                   segment has been previously narrowed by degeneration;
                   compression shear of articular cartilage may occur with
                   capsular stretch.

            2. Hyperextension sprain (ETK)
                  a. Pt remembers hyperextension episode, with or without
                  rotation.
                  b. Extension with or without rotation is most painful; flexion
                  is better movement.
                  c. Short term pathology; usual sequelae of collagenous
                  capsular damage. Additional pathology of hyperextension
                  may be articular cartilage damage (cartilage damage may
                  "extend the life" of inflammatory response due to collagen
                  degradation cycle; hyperextension may also impinge
                  posterior capsule.
                  d. Long term pathology = muscle fatigue due to antalgic
                  posturing in flexion.

            3. Facet joint capsular impingement (ETK) - This pathology can be
            the result of trauma with excessive force but often occurs with slight
            (some would say normal) movements. It is included here because
            it usually occurs with a sudden onset. Impingement occurs when a
            portion of the joint capsule becomes folded and entrapped inside
            the joint. It can be part of the synovial lining, and some call it a
            "meniscoid body". A meniscoid body is part of the synovial
            structure. Twomey has suggested "meniscoid bodies" are
            detachment of the multifidus mm from previous injuries. (A slip of
            the multifidus muscle often blends with the joint capsule much like
            the rotator cuff muscles at the shoulder).
                    a. Immediate pathology = release of pain producing
                    substance; irritation of joint capsule (one of the most
                    mechano-sensitive tissues when inflamed). Antalgic
                    positioning and movement. Often patient will attempt to self
                    manipulate and pinch the capsule more. Gradual recovery
                    over time with capsule "wiggling" its way out of the capsule.
                    b. Long term pathology = antalgic posturing and movement
                    can establish pain/spasm cycle in guarding muscles.
                    (c). Degeneration narrows the disk space and facet joint
                    capsules can slacken. This may make impingement more
                    likely.

      E. Nerve injury
            1. Central nervous system structures
                   a. In hyper-mobile persons, hyper-flexion can traction the
                   spinal cord without serious damage to the segments.
                   http://www.medmedia.com/o11/176.htm
PHYT 6202 - Basic Spinal Tissue Pathophysiology                                   7


                         (1). Immediate pathology = spinal cord shock;
                         bleeding and inflammation among fibers of cord
                         (2). Long term pathology = muscle paresis or
                         paralysis; diminished or absent sensation and
                         neurological control
                  b. Large central traumatic protrusion can pressure the
                  spinal cord or cauda equina.
                         (1). Immediate pathology = pressure disturbance in
                         conduction through cord (cervical and thoracic) can
                         be as minor as tingling in hands and feet or as major
                         as paralysis: cauda equina in lumbar area (tingling to
                         loss of sensation and motor power; loss of bowel and
                         bladder)
                         (2). Long term pathology= as above

            2. Peripheral nerve injury
                  a. Traction or Compression of nerve plexus (usually the
                  brachial plexus) -.(NTK) AKA burner syndrome
                  http://www.medmedia.com/t1/150.htm
                         (1). Mechanisms – Head/neck side flexion with
                         ipsilateral shoulder depression; hyper side flexion to
                         same side; shoulder hyper abduction with traction.
                         (2). Immediate pathology = injury to collagenous
                         elements; swelling; actual destruction or
                         dissassociation of nerve fibers; slowing or altering
                         conduction.
                         (3). Long term pathology - Study showed that 70%
                         of college football players had residual symptoms.


                  b. Nerve root injury
                        (1). Injury mechanism = Closing of spinal canal by
                        disk (thoracic and lumbar); Closing of intervertebral
                        foramen by disk, facet, descending pedicle (all areas)
                        (2). Immediate pathology
                                (a). Injury to collagenous elements produce
                                swelling. Swelling affects myelin slowing or
                                elimination of conduction from myelinated
                                fibers. Direct mechanical stimulation creates
                                messages as if fiber were conducting from the
                                receptor. Can create imbalance at “gate”
                                favoring C fiber input.
                                (b). Nerve root ischemia – traumatic incident
                                may injure blood supply slowing or limiting its
                                ability to heal. The nerve is contained within a
                                somewhat unyielding fibrous sheath. As nerve
                                swells, it may compromise its own blood
PHYT 6202 - Basic Spinal Tissue Pathophysiology                                      8


                                  supply. Ischemic nerve root are acutely
                                  mechano sensitive. (See Kessler, p. 552-3
                                  plus ligature article by Smyth and Wright)
                           (3). Long term pathology
                                  (a). Collagenous scar may form within the
                                  nerve or around the nerve (adhesion to less
                                  yielding tissues in the area); may lead to
                                  decreased nerve excursion (attempts to
                                  elongate nerve to its normal length renders
                                  nerve ischemic).
                                  (b). Collagenous tissue element (as opposed
                                  to the conductive tissue) may remodel short.
                                  (attempts to elongate nerve to its normal length
                                  renders nerve ischemic)..

      F. Posterior Muscle Injury (ETK)
            1. Mechanism = Strain: eccentric hyper-flexion or flexion c rotation;
            strong isometric while in flexion or flexion c rotation; lifting injuries.
            Hyper-flexion phase of whiplash; Contusion: direct blow to
            muscles; Surgical incisions
            2. Short term pathology = Strains are usually more of a
            collagenous injury and follow that path; Contusions can be more
            injury to contractile part and there would be more bleeding and
            repair of contractile portion with fibrous scar.
            3. Long term pathology
                    a. Pain/spasm cycle -
                    b. Fibrous scar and adhesions
                    c. Muscle weakness and endurance – decreased ability to
                    perform functional movements; painful fatigue with “normal
                    range loading”.
                    d. Muscle imbalance – joints work with faulty PICR
                    e. Deficient joint stabilization

V. Postural Pathology
      A. Mechanisms - inherited, congenital, habitual, acquired, vocational,
      avocational repetitive postures and movements cause muscles and other
      supporting tissues to remodel with excessive length, diminished length,
      less than normal strength, greater than normal strength.
             1. Well-recognized total body patterns in the sagittal plane (Think
             of these as forms of column buckling under the constant downward
             pressure of gravity)
                    a. Hyperlordotic/Hyperkyphotic
                    b. Sway back
                    c. Flat back
             2. Well-recognized sagittal head/neck/shoulder postures
PHYT 6202 - Basic Spinal Tissue Pathophysiology                                     9


                   a. Forward head c excessive lordosis; often part of Hyper-
                   lordotic/Hyper-kyphotic pattern.
                    b. Forward head c straight neck and posterior cranial
                   rotation; shoulder protraction; often part of sway back.
            3. Well-recognized frontal/horizontal patterns
                   a. Unilateral short leg (actual and functional)
                   b. Scoliosis - http://www.medmedia.com/o11/59.htm
                   c. Torticollis - side flexion- rotation opposite in cervical spine
                   - http://www.medmedia.com/o11/124.htm
      B. Early Pathology
            1. Accumulation of fatigue waste products in tissues; especially
            constantly contracting muscles; creep in collagenous tissues that
            are maintained in elongated state (breaking of bonds; denaturing of
            collagen); stress deprivation in tissues constantly on slack.
            2. Stress deformation of articular cartilage surfaces held in
            constant contact
      C. Late Pathology
            1. Collagen remodeling either with excessive length or diminished
            length depending on demand.
            2. Shift in length-tension curve in contractile element
                   a. Lower peak force/earlier if muscle used in shorter range
                   b. Higher peak force/later if muscle used in excessive length
                   range.
            3. Postural dysfunctions may be related to degenerative conditions
                   a. Hyperlordotic/Hyperkyphotic -
                             (1). may increase forward shearing forces in lordotic
                             areas (cervical and lumbar area to encourage the
                             development of degenerative spondlyolithesis
                           http://www.medmedia.com/o11/106.htm
                           (2). Facet joint fatigue or chronic sprain
                                  (a). Special designation used to describe pain
                                  that seems to emanate from the facet joints but
                                  the mechanism is not traumatic.
                                  (b). Assumed to be related to chronic overuse
                                  in repetitive twisting of the spine and chronic
                                  postural hyper-compression sprain. Often
                                  worse in pts with advanced segmental
                                  degeneration.
                    b. Flat back -
                           (1). Chronic loading of lumbar spine in flexion may
                           lead to gradual degeneration of posterior annulus due
                           to constant backward pressure of the nucleus

                    c. Sway back
                          (1). Chronic facet joint compression fatigue at lumbo-
                          sacral junction; flexion degeneration of disk above
                          lowest level
PHYT 6202 - Basic Spinal Tissue Pathophysiology                               10


                    d. Forward head c straight neck
                          (1). Compression fatigue in upper cervical areas.
                          (2). Disk degeneration at lower levels
                    e. Forward head c lordosis
                          (1). Facet joint compression fatigue in middle
                          segments
                          (2). Encourages forward shear at segments

VI. Degenerative Pathology
      A. Basic Assumption regarding the Spinal Segments. The natural history
      of the intervertebral segment is that all humans develop
      degenerative segments that first become unstable and then
      eventually become re-stabilized. Some persons may be genetically
      predisposed to accelerated degeneration and development of
      symptoms. (Tissue turnover, shape of spinal canal, asymmetrical
      facets, pain suppression deficiency, postural dysfunction, etc.)
      Some may acquire conditions through life that accelerated
      degeneration and create symptoms (disk tear, facet joint
      hypomobility, hypermobility, and hypertrophy; de-conditioning,
      postural dysfunction. Most undergo this process with tolerable
      symptoms. http://www.medmedia.com/lib6/107.htm
      2. Almost any pathology that can result from trauma, can result from
      similar mechanisms repeated with lighter forces given enough time and
      cycles of application.

VII. Degenerative pathology of the anterior elements
      A. Osteophytes of the vertebral body
            1. Mechanism - instability and disk space narrowing cause
            ligaments and annulus to slacken; instead of tightening gradually,
            they tighten suddenly subjecting attachments to stress. Bone will
            hypertrophy at site of attachment as a stress reaction.
            2. Long-term pathology
                    a. Anterior osteophytes - Often causes no painful pathology
                    when osteophytes are anterior because they do not press on
                    pain producing structures. Are often misleading in
                    radiographs (false positive for serious pathology)
                    Occasionally persons with anterior osteophytes in the neck
                    have voice changes and have difficulty swallowing. Anterior
                    osteophytes in the lumbar spine can irritate the descending
                    aorta. Anterior body osteophytes have been known to friction
                    the sympathetic chain in the thoracic spine.
                    b. Posterior osteophytes – Have the greatest potential for
                    causing pathology. Can pressure neural structures in the
                    central canal or in the intervertebral foramen. Are often a
                    contributor to central or lateral spinal stenosis.
PHYT 6202 - Basic Spinal Tissue Pathophysiology                                    11


                    c. Lateral osteophytes - osteophytes developing off the
                    joints of von Lushka in the cervical spine can have pressure
                    on the vertebral artery which can cause drop attacks.

      B. Anterior longitudinal ligament remodeled with excessive length
            1. Mechanism = chronic Hypl-Hypk postural dysfunction;
            hyperextension injury.
            2. Short term pathology = allows forward shear of top vertabra
            relative to bottom; facet joint irritation; loss of one of many controls
            over rotation.
            3. Long term pathology
                    a. With forward shear at segment and chronic hyper-
                    compression, facet joints become pathological with synovial
                    hypertrophy; hypermobility; cartilage wear; and hypertrophy;
                    facet joint hypertrophy can (along with other pathology)
                    narrow IVF and pinch nerves.

      C. Degenerative inter-vertebral disk pathology
           1. Mechanism = http://www.medmedia.com/lib3/213.htm
                 a. Natural history of disk, i.e., nucleus becomes more
                 fibrous; collagen turn over slows so slight damage is not
                 repaired.
                 b. Habits, occupation, body mechanics that distribute
                 pressure of nucleus unevenly on annulus.
                         (1). Chronic HypL-HypK standing posture - Anterior
                         protrusion
                         (2). Sitting, repeated bending, flat back posture -
                         Posterior protrusion
                         (3). Occupations or sports with repeated rotation.
                 c. Assymetry of segmental movement
                         (1). Unilateral facet hypomobility
                         (2). Unilateral facet hypermobility
                         (3). Assymetrical facets
                         (4). Adjacent to hypomobile segments
                 d. Loss of control over rotation
                         (1). Abdominal oblique weakness
                         (2). Multifidus weakness
                         (3). Excessive ligament length

             2. Internal disk disruption – AKA “black disk disease” because of
             its appearance on certain MRI studies due to loss of water content.
                    a. Accelerated aging of the disk
                    b. End plate disruption – diminished nutrition of the disk
                    c. Cracks and fissures in the annulus
                    d. Nucleus Pulposus becomes more fibrotic; loses GAGs
                    and does not bind water.
PHYT 6202 - Basic Spinal Tissue Pathophysiology                                     12


                   e. Usually allows disk space to narrow; annulus slackens;
                   ligaments slacken (at least temporarily); segment becomes
                   unstable with A-P shear and rotary shear. Pathology is
                   usually from the other segmental structures that undergo
                   strain due to loss of stability (facets, facet joint capsules,
                   ligaments, etc).
                   f. Nucleus may or may not herniated the annulus

            3. Disk disruption with herniation (Posterior lateral is shown but
            herniation can occur in other part of the disk)
                   a. Normal Disk
                                         (1). Annulus contains nucleus
                                         pulposus under pressure
                                                (a). NP is constantly trying to
                                                expand
                                                (b). A condition that exists in
                                                the first 4-5 decades
                                                (c). Disk is a ligament that helps
                                                control rotation and shear.


                   b. Early Pathology
                                 (1). Stage 1 - Develops gradually as radial
                                 and circumferential tears develop in the disk
                                 due to faulty mechanics and overstress.
                                        (a). Disk may become mildly
                                        symptomatic - intermittent back pain;
                                        often assymptomatic.
                                        (b). Disk is less able to control rotation
                                        and shear; other segmental structures
                                        may become symptomatic.

                                  (2). Stage 2 - Nucleus pulposus is contained
                                  by the annulus under great pressure;
                                  gradually works its way peripherally through
                                  the annulus.
                                          (a). Annulus bulges when disk is
                                          compressed under pressure and may
                                          produce symptoms. When not
                                          compressed may be symptomatic
                                          (b). Disk is disrupted and may allow
                                          abnormal shear or rotation; symptoms
                                          from other segmental structures.
                                  http://www.medmedia.com/a5/115.htm
PHYT 6202 - Basic Spinal Tissue Pathophysiology                                  13


                                  (3). Stage 3 (annular bulge) - NP actually
                                  causes a peripheral bulge. At this point disk
                                  pathology usually becomes symptomatic.
                                  Proteolytic enzymes from cartilage damage
                                  and pain producing substances from collagen
                                  damage irritate pain sensitive tissues that are
                                  toward the periphery of the disk. Ligament
                                  tissue may be irritated, dura and nerve
                                  sleeve.

                          (4). When disk bulge reaches stage 3 they can take
                         three basic sizes
                                 (a). Small (intermittent)
                                 (b). Medium (intermittent and constant)
                                 (c). Large (usually constant)
                         (5). Annular bulge can occur in three locations of a
                         disk
                                 (a). Anterior disk protrusion (ADP) - The NP
                                 may work its way anteriorly in which case it
                                 may be somewhat benign in terms of directly
                                 producing symptoms but not benign in terms of
                                 producing secondary symptoms related to
                                 segmental instability.
                                 (b). Near Lateral Postero-lateral disk
                                 protrusion - The NP may work toward postero-
                                 lateral disk just lateral to the posterior lateral
                                 ligament. This location is said to comprise 80%
                                 of the immediate symptom producing DP's.
                                 (c). Far Lateral Postero-lateral disk protrusion
                                 - Protrusion occurs more lateral than Near
                                 Lateral and produces slightly different
                                 symptoms and different prognosis.
                         (6). Near Postero-lateral protrusions can sequentially
                         pressure and friction the following structures with
                         resulting inflammatory signs and symptoms:
                         Posterior Longitudinal Ligament, Dura, Dural sleeve,
                         nerve root.
PHYT 6202 - Basic Spinal Tissue Pathophysiology                                  14


                               (7). Stage 4 - Annulus ruptures. NP extrudes or
                               becomes sequestrated. (More common in L/S less
                               common in C/S due to wider ligament; less room to
                               accommodate large protrusion; pt's seek treatment
                               earlier).




                                   (a). Early pathology for stage 4 - Nucleus
                                  material is interpreted as a "foreign body" and
                                  causes a strong inflammatory reaction by the
                                  immune cells in the area. Since that area is
                                  around the nerve root it often causes intense
                                  discomfort from the nerve root. Because the
                                  NP is a softer object frictioning the nerve root
                                  there is some relief from the pathology
                                  associated with pressure and frictioning of the
                                  nerve root.
                                  (b). Long term pathology - since it is
                                  interpreted as a foreign object, the NP is
                                  completely digested and dissolved.
                                  Unfortunately a fibrous scar can be left to
                                  adhere the nerve root to surrounding
                                  unyielding tissues.
            4. Not all disk postero-lateral protrusions cause symptoms. There
            is not a direct correlation between severity of a patient's disk
            degeneration and signs and symptoms produced.
            http://www.medmedia.com/lib6/107.htm
                    a. Reasons assymptomatic or symptomatic PL HNP may be:
                          (1). Size of spinal canal
                          (2). Size of intervertebral foramen
                          (3). Shape and size of pedicles
                          (4). Pre-existing instability
                          (5). Pre-existing degeneration
                          (6). Pain suppression abilities
                          (7). Postural dysfunction

            5. Late Pathology of disk protrusion
                  a. The disk is as much a ligament helping control rotation at
                  the segment as much as a separator between vertebra.
                  Loss of control over rotation will subject the facet joints to
                  increased pressure and probable degeneration. The same
                  is true for strain on ligaments controlling rotation. If over
                  rotation occurs the nerve roots can be damaged.
PHYT 6202 - Basic Spinal Tissue Pathophysiology                                  15


                    b. As nucleus moves toward the periphery or is lost through
                    a tear in the annulus, the disk space narrows; pedicles
                    descend, IVF narrows, ligaments and annulus slacken.
                    c. Continued pressure on nerve root by a bulging annulus
                    can change its conductivity permanently.
                    d. Cartilage degeneration produces vigorous inflammation
                    that eventually heals with scar tissue. The scar tissue can
                    cause adhesions between nerve roots and surrounding
                    structures.

             6. Discitis – infection of the disk
                   a. Systemic – organism introduced to disk by circulation
                   b. Iatrogenic – post discogram; partial disectomy
                   c. Inflammation and repair of the disk
                            (1). Disk could expand posteriorly into spinal canal to
                            cause neural signs and symptoms.
                            (2). Segment usually left with narrowing and
                            instability.

      D. Anterior muscle weakening, decreased endurance, length changes.
            1. Degenerative process causes discomfort; discomfort often
            reduces activity level
            2. Imbalance develops between key muscles that exert mutual
            control. These are the abdominals with hip flexors and deep neck
            flexors with sterno-mastoid (former gets weak and elongated, later
            gets tight and strong). This imbalance encourages A-P shearing at
            segments.
            3. Muscle helping ligaments, disk and facets control rotation
            weaken with avoidance of movement. Loss of this control over
            rotation puts greater load on other rotation control structures and
            they in turn fail.

VIII. Degenerative pathology of the posterior elements.
       A. Pedicles
            1. Upper pedicle descends toward the lower as disk space
            narrows. Since nerve roots are directly under the pedicle, it
            becomes a source of pressure.
            2. Pedicles hypertrophy; perhaps because of excessive pressure

      B. Degenerative Spondylolythesis – AKA osteoarthritis, spondylosis, DJD
      of the segment; Intermittent Lateral stenosis; Central stenosis.
             1. Disk disruption; slackening of ligaments; change in shape of
             facets. Usually L4 slips forward on L5 (posterior neural arch intact).
             2. Narrows both central canal and intervertebral foramen not
             usually a part of the segmental degeneration process of DJD
             development.
PHYT 6202 - Basic Spinal Tissue Pathophysiology                                    16


             3. Can be subtle and easily manageable by PT or severe requiring
             surgical decompression and/or stabilization.

      C. Facet joint capsular hypertrophy
            1. With disk space narrowing, facet joint capsules slacken and
            "bunch up".
            2. With excessive pressure on articular cartilage there is flaking of
            collagen. Synovial tissue reacts and must be excessively active.
            (It is synovial tissue's job to keep joint fluid clear of collagen during
            normal turnover of articular cartilage). Since tissue is hyperactive it
            hypertrophies. Assumed to be more prone to impingement.
            3. Synovial cyst – pinching enlargement of synovial cycle with
            accumulation of fluid in cyst. Can be large enough to cause nerve
            pressure.

      D. Facet joint articular cartilage osteoarthritis
            1. With excessive pressure and abrasion of articular cartilage with
            segmental instability, there is more articular cartilage damage than
            occurs with normal turnover.
            2. Articular cartiage thins, develops fissures and may erode
            completely.

      E. Facet joint bony hypetrophy – AKA “re-stabilization”
            1. A response to articular cartilage thinning is bony hypertrophy
            under the cartilage. Bone becomes more dense under the
            cartilage.
            2. Another typical osteoarthritis response due to joint instability is
            for the joint surface to broaden, to make more surface area. This is
            seen as an attempt to "re-stabilize" the joint.
            3. Broadening of the joint surface is around the edges and are
            often called osteophytes. Osteophytes of the facet joints are often
            a source of intervertebral narrowing which can subject the nerve
            root to trauma.

      F. Slackening of ligaments
            1. With disk space narrowing ligaments slacken. If a collagenous
            tissue slackens it normally remodels short and "re-tightens" but at a
            shorter length.
            2. Because the segment is slack and often shifts pulling sharply on
            ligaments, it is assumed that this keeps ligaments from remodeling
            short and helping re-stabilize the segment. Of course, if posterior
            ligament does remodel short it would increase lordosis and help to
            narrow the intervertebral segment.
            3. Slack ligaments allows shearing and excessive rotation.
            4. Ligamentum flavum - One ligament that is usual is the
            ligamentum flavum. This ligament folds inward between the lamina
PHYT 6202 - Basic Spinal Tissue Pathophysiology                                 17


             and can narrow the spinal canal subjecting either the spinal cord or
             cauda equina to pressure. One of many elements causing central
             or lateral stenosis.

IX. Segmental Instability
      1. Segmental stability is the result of optimal function of three
      interdependent subsystems
             a. The passive subsystem – Ligaments, bone, disk, facets
             b. The active subsystem – muscles
                     (1). Deep intersegmental muscles
                     (2). More superficial global muscles
             c. The neural subsystem – The motor commands from the CNS
             that gives muscles their proper amplitude and relative timing.
             d. Gross deficiency in any one system leads to gross instability.
             e. Subtle deficiencies in any one sub-system can be compensated
             by up-regulation of the others (the basis of exercise therapy).
             f. Subtle deficiencies un-compensated can lead to segmental
             degeneration.
      2. The neutral zone concept (not to be confused with the neutral spine
      position).
             a. A small area somewhere between the extremes of motion in
             each degree of freedom of segmental motion.
             b. Passive structures and global muscle control the spine (limit
             excessive or possibly injurious movement outside the neutral zone.
             In doing they set the limits of the neutral zone.
             c. Intersegmental muscles control the spine in the neutral zone,
             i.e., they can stiffen or let loose the segment appropriate for the
             activity.
             d. Injury or poor function of these structures allows an expansion of
             the neutral zone. Intersegmental muscles are required to control a
             larger movement and sometimes this demand is greater than their
             capability.
             e. Dysfunction of intersegmental muscles allows for poor control of
             movement in the neutral zone. This can be a subtle source of
             stress and strain on segmental tissues leading to pain and
             degeneration.
             f. Global and local (intersegmental) muscles should be coordinated
             in action with the global muscles moving the spine or controlling
             large forces applied to the trunk while the local muscles stabilize
             the segment.
      3. Post-surgical Instability
             a. Some types of discotomy without fusion cause a decrease in
             disk height creating segmental instability.
              b. Surgery is performed even with fusion of a segment. If patient
             keeps same muscle tightness and weakness patterns as
             pre-surgery two things may happen:
PHYT 6202 - Basic Spinal Tissue Pathophysiology                                    18


                    (1). Surgery fails after initial success.
                    (2). Segments above or below undergo excessive stress
                    inducing instability.

X. De-conditioning
      A. Relative de-conditioning – a state where muscles and other tissues
      lack strength/endurance; length required of usual ADL, the persons
      chosen IADLs plus a reserve for emergencies.
      B. Morbid de-conditioning – a state where muscles and other tissues
      lack strength/endurance; length required of usual ADLs so that performing
      ADLs is dangerous to homestasis.
      C. Spinal Pathology related to deconditioning
             1. Segmental instability and degeneration
             2. Postural dysfunction
             3. Movement dysfunction
             4. Delayed muscle soreness
             5. Muscle strain or ligament sprain

XI. Dysfunctional movement
       A. Movement habits or patterns that have been related to risk of injuring
       spinal tissues. Activities often requiring modification.
              1. Supine to sit
              2. Floor to waist lift
              3. Overhead lift
              4. Reaching forward or forward and down
              5. Bending forward
              6. Sitting working at a desk
              7. Sit to stand
              8. Sitting posture
              9. Standing posture
              10. Lying postures
              11. Turning while holding an object of weight.
              12. Entering and exiting a car.
              13. IADLs as required.

XII. Systemic pathology – pathologies that can cause spinal pain. PT either
modifies plan considering pathology or makes the appropriate referral.
       A. Cervical, Abdominal, Thoracic, and Pelvic organ disease
PHYT 6202 - Basic Spinal Tissue Pathophysiology                               19


      B. Cardio-vascular disease
      C. Neurological and disease
      D. Obesity
      E. Deconditioning
      F. Cancer and metasteses
      G. Depression
      H. Chronic fatigue
      I. Chronic Pain Conditions
            1. Failure of pain suppression mechanisms
                   a. Peripheral – changes in the posterior horn whereby wide
                   dynamic range fibers conduct pain only.
                   b. Central failure – exhaustion of or failure to produce
                   sufficient endorphins, enkephalins, etc.
            2. Myofascial Pain Syndrome
            3. Fibromyalgia
            4. Failed Back Surgery Syndrome
                   a. Causes
                           1. Nerve root scarring (inside canal, intervertebral
                           foramen, intermuscular)
                           2. Arachnoiditis - inflammation of meniges
                           3. Segmental instability (degeneration above or
                           below fusion)
                           4. Psycho-emotional response in patient who was not
                           a good candidate
            5. Low Back Pain Syndrome
                   a. Psycho-emotional disorder typified by pain and suffering
                   behaviors.
                   b. Physical source cannot be found by usual investigative
                   means.
                   c. Sometimes responds to psycho-therapy, relaxation
                   training, myo-fascial treatment, patient education, job
                   retraining and eventually leading to exercise reconditioning.

				
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